Abstract
Recurrent vulvovaginal candidosis (RVVC), defined as three or more episodes of vulvovaginal candidosis (VVC) within a 12-month period, is a common and debilitating condition that affects a significant percentage of reproductive-aged women, negatively impacting their quality of life. This review aimed to synthesize the most recent scientific data on the pathophysiological mechanisms triggering primary or idiopathic RVVC. Three databases (PubMed, Scopus, and Web of Science) were searched for studies published between 2014 and 2024. Twelve studies were included, covering prospective cohort, cross-sectional, and case-control studies conducted in different countries. The results indicate that recurrence may be related to both intrinsic characteristics of the pathogen, such as increased virulence attributes of Candida spp., and host immune system dysregulation, including alterations in Th1/Th17 and Th2/Treg cytokine levels, decreased levels of mannose-binding lectin (MBL), impaired neutrophil and lymphocyte function, and overexpression of CD163+ macrophages and NLRP3 inflammasome. Additionally, genetic factors, such as polymorphisms in the MBL2, IL-12, NLRP3, and TLR2 genes, are associated with increased susceptibility to RVVC. In conclusion, RVVC appears to involve a complex interaction between pathogen virulence and an altered host immune response, which reinforces the need for further investigations to develop personalized therapeutic strategies.